ArticleJournal of molecular and cellular cardiology2013
T-type Ca²⁺ channels regulate the exit of cardiac myocytes from the cell cycle after birth.
Article in Journal of molecular and cellular cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- High-content phenotypic assay for proliferation of human iPSC-derived cardiomyocytes identifies L-type calcium channels as targets.Journal of molecular and cellular cardiology · 2019Article
- Calcium Channels in Postnatal Development of Rat Pancreatic Beta Cells and Their Role in Insulin Secretion.Frontiers in endocrinology · 2018Article
- Endostatin is protective against monocrotaline-induced right heart disease through the inhibition of T-type Ca(2+) channel.Pflugers Archiv : European journal of physiology · 2016Article
- Article
- Endostatin inhibits T-type Ca2+ channel current in guinea pig ventricular myocyte.The Journal of veterinary medical science · 2015Article
- Caveolin-3 Overexpression Attenuates Cardiac Hypertrophy via Inhibition of T-type Ca2+ Current Modulated by Protein Kinase Cα in Cardiomyocytes.The Journal of biological chemistry · 2015Article
- Origin of cardiomyocytes in the adult heart.Circulation research · 2015Review
- Article
- Isolated human uterine telocytes: immunocytochemistry and electrophysiology of T-type calcium channels.Histochemistry and cell biology · 2015Article
- Role for the TRPV1 channel in insulin secretion from pancreatic beta cells.The Journal of membrane biology · 2014Article
- Cav3 T-type channels: regulators for gating, membrane expression, and cation selectivity.Pflugers Archiv : European journal of physiology · 2014Review
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledT-type Ca(2+) channels (TTCCs) are expressed in the fetal heart and then disappear from ventricular myocytes after birth. The hypothesis examined in this study was the α1G TTCCs' influence in myocyte maturation and their rapid withdrawal from the cell cycle after birth.
methodsCardiac myocytes were isolated from neonatal and adult wild type (WT), α1G-/- and α1G over expressing (α1GDT) mice. Bromodeoxyuridine (BrdU) uptake, myocyte nucleation, cell cycle analysis, and T-type Ca(2+) currents were measured.
resultsAll myocytes were mono-nucleated at birth and 35% of WT myocytes expressed functional TTCCs. Very few neonatal myocytes had functional TTCCs in α1G-/- hearts. By the end of the first week after birth no WT or α1G-/- had functional TTCCs. During the first week after birth about 25% of WT myocytes were BrdU+ and became bi-nucleated. Significantly fewer α1G-/- myocytes became bi-nucleated and fewer of these myocytes were BrdU+. Neonatal α1G-/- myocytes were also smaller than WT. Adult WT and α1G-/- hearts were similar in size, but α1G-/- myocytes were smaller and a greater % were mono-nucleated. α1G over expressing hearts were smaller than WT but their myocytes were larger.
conclusionsThe studies performed show that loss of functional TTCCs is associated with bi-nucleation and myocyte withdrawal from the cell cycle. Loss of α1G TTCCs slowed the transition from mono- to bi-nucleation and resulted in an adult heart with a greater number of small cardiac myocytes. These results suggest that TTCCs are involved in the regulation of myocyte size and the exit of myocytes from the cell cycle during the first week after birth.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.